ArticleAging cell2022
Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- Trial
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Loss of sirtuin 3 disrupts cellular senescence signaling pathways.GeroScience · 2026Article
- Article
- Necroptosis induced by MLKL overexpression in liver triggers cellular senescence and leads to chronic inflammation and fibrosis.GeroScience · 2026Article
- SOD1 deficiency drives ferroptosis-linked oxidative and reproductive aging, mitigated by ginseng root extract.GeroScience · 2026Article
- Rhapontigenin alleviates cellular senescence and physiological aging by upregulating sirt1 and promoting autophagy.Chinese medicine · 2026Article
- Remodeling of senescent macrophages in synovium alleviates trauma- and aging-induced osteoarthritis.Bioactive materials · 2026Article
- Resveratrol delays senescence of human dental pulp stem cells via activating the SIRT1-mitochondrial autophagy.Scientific reports · 2025Article
- Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025Review
- The effect of enhanced glycolysis on cardiac aging.GeroScience · 2025Article
- Targeting Senescence in Oncology: An Emerging Therapeutic Avenue for Cancer.Current oncology (Toronto, Ont.) · 2025Review
- Article
- A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice.Nature aging · 2025Article
- A novel necroptosis-related miRNA signature for predicting the prognosis of esophageal cancer and immune infiltration analysis.Translational cancer research · 2025Article
- Necrostatin-1 alleviates temporomandibular joint osteoarthritis and inhibits chondrocyte senescence and necroptosis possibly via p53/ MAPK downregulation.Frontiers in bioengineering and biotechnology · 2025Article
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Therapeutic strategies of targeting non-apoptotic regulated cell death (RCD) with small-molecule compounds in cancer.Acta pharmaceutica Sinica. B · 2024Review
- Senolytic treatment does not mitigate oxidative stress-induced muscle atrophy but improves muscle force generation in CuZn superoxide dismutase knockout mice.GeroScience · 2024Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
The goal of this study was to test the role cellular senescence plays in the increased inflammation, chronic liver disease, and hepatocellular carcinoma seen in mice null for Cu/Zn-Superoxide dismutase (Sod1KO). To inhibit senescence, wildtype (WT) and Sod1KO mice were given the senolytics, dasatinib, and quercetin (D + Q) at 6 months of age when the Sod1KO mice begin exhibiting signs of accelerated aging. Seven months of D + Q treatment reduced the expression of p16 in the livers of Sod1KO mice to WT levels and the expression of several senescence-associated secretory phenotype factors (IL-6, IL-1β, CXCL-1, and GDF-15). D + Q treatment also reduced markers of inflammation in livers of the Sod1KO mice, for example, cytokines, chemokines, macrophage levels, and Kupffer cell clusters. D + Q treatment had no effect on various markers of liver fibrosis in the Sod1KO mice but reduced the expression of genes involved in liver cancer and dramatically reduced the incidence of hepatocellular carcinoma. Surprisingly, D + Q also reduced markers of necroptosis (phosphorylated and oligomerized MLKL) in the Sod1KO mice to WT levels. We also found that inhibiting necroptosis in the Sod1KO mice with necrostatin-1s reduced the markers of cellular senescence (p16, p21, and p53). Our study suggests that an interaction occurs between cellular senescence and necroptosis in the liver of Sod1KO mice. We propose that these two cell fates interact through a positive feedback loop resulting in a cycle amplifying both cellular senescence and necroptosis leading to inflammaging and age-associated pathology in the Sod1KO mice.
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